Case Report
Iatrogenic Wernicke Encephalopathy in a Patient With Severe Hyperemesis Gravidarum Lauren E. Giugale, MD, Omar M. Young, MD, and David C. Streitman,
MD
BACKGROUND: Hyperemesis gravidarum complicates 0.5–2.0% of pregnancies and may lead to substantial nutritional deficiencies. Total parenteral nutrition can be used in severe cases in an attempt to avoid such deficiencies. Rarely, thiamine deficiency resulting in Wernicke encephalopathy occurs, with significant maternal morbidity. CASE: We present the case of a 30-year-old woman with hyperemesis gravidarum at 13 4/7 weeks of gestation treated with prolonged total parenteral nutrition that lacked thiamine supplementation, resulting in iatrogenic Wernicke encephalopathy. After high-dose intravenous thiamine repletion, she experienced slow resolution of her symptoms. CONCLUSION: Pregnancies complicated by hyperemesis gravidarum treated with total parenteral nutrition represent potential high-risk clinical scenarios for thiamine deficiency. Compositions of total parenteral nutrition are not standardized. Thus, physicians must confirm repletion of all essential components to avoid significant morbidity. (Obstet Gynecol 2015;125:1150–2) DOI: 10.1097/AOG.0000000000000557
H
yperemesis gravidarum, a severe form of pregnancy-associated nausea and vomiting, affects 0.5–2.0% of all pregnancies.1 Symptoms of hyperemesis gravidarum include the following: persistent vomiting, ketonuria, weight loss of at least 5% of prepregnancy
From the Department of Obstetrics, Gynecology and Reproductive Sciences and the Division of Maternal-Fetal Medicine, Department of Obstetrics, Gynecology and Reproductive Sciences, Magee-Womens Hospital and University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania. Corresponding author: Lauren E. Giugale, MD, Department of Obstetrics, Gynecology and Reproductive Sciences, Magee-Womens Hospital and University of Pittsburgh Medical Center, 300 Halket Street, Pittsburgh, PA 15213; e-mail: [email protected]. Financial Disclosure The authors did not report any potential conflicts of interest. © 2015 by The American College of Obstetricians and Gynecologists. Published by Wolters Kluwer Health, Inc. All rights reserved. ISSN: 0029-7844/15
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Teaching Points 1. Hyperemesis gravidarum requiring total parenteral nutrition should be considered a high-risk clinical scenario for nutritional deficiency. 2. Total parenteral nutrition is not standardized; physicians must take responsibility to ensure that a multivitamin, including thiamine, is incorporated in the treatment of hyperemesis gravidarum. 3. This case report adds to the known risks associated with total parenteral nutrition delivered through a peripherally inserted central catheter in pregnancy, and further supports the goal of using alternative methods to provide nutrition in this setting.
weight, electrolyte disturbances, and abnormalities of thyroid and liver function tests.1 In refractory hyperemesis, obstetricians may use total parenteral nutrition (TPN) to improve maternal nutritional status until the patient is able to tolerate oral alimentation. Rarely, Wernicke encephalopathy can result from nutritional thiamine deficiency in the setting of severe hyperemesis gravidarum.2–5 We present a case of Wernicke encephalopathy that developed secondary to lack of thiamine repletion during the course of TPN therapy and aim to underscore the nature of thiamine deficiency in the current case and the need for the selective and judicious use of TPN in pregnancy.
CASE A 32-year-old woman, gravida 4 para 2101 presented to an outside hospital at 13 2/7 weeks of gestation with persistent lethargy, weakness, ataxia, and blurred vision. Notably, she had been diagnosed with hyperemesis gravidarum at approximately 8 weeks of gestation. The condition was not controlled with conservative management, and TPN was initiated through a peripherally inserted central catheter. After 28 days of continuous TPN, she noted 7 days of subjectively worsening lethargy, blurred vision, and weakness requiring assistance with ambulation. Notably, all three prior pregnancies were complicated by hyperemesis gravidarum requiring hospitalization; she had received TPN only in her most recent antecedent pregnancy. Initial laboratory evaluation demonstrated normal electrolytes, anemia (hemoglobin 8.5 gm/dL), and mild thrombocytopenia (platelets 1453109/L). An electroencephalogram demonstrated dysrhythmia and diffuse delta activity, indicative of a moderate encephalopathy. A lumbar puncture and magnetic resonance imaging of the brain and neck were all negative. Before transfer to our facility at 13 4/7 weeks of gestation, her TPN was discontinued and she was given intravenous folic acid and thiamine supplementation.
OBSTETRICS & GYNECOLOGY
Copyright ª by The American College of Obstetricians and Gynecologists. Published by Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
On arriving at our institution, a neurologic examination was notable for psychomotor slowing. Although the patient’s cranial nerves were intact and symmetric, she exhibited prominent bilateral gaze-evoked nystagmus. Strength and sensory testing were normal, but coordination testing demonstrated slowing of finger-to-nose testing in bilateral upper extremities with mild right-side ataxia. Her gait was widebased, wavering, and unsteady. She was unable to stand upright in place for greater than 2 seconds and she could ambulate only with a two-person assist. Repeat electroencephalography was performed given these persistent encephalopathic features and again revealed generalized slowing consistent with a diffuse disturbance of cerebral function. Thiamine levels drawn at the outside hospital and at our institution returned critically low values of less than 7 nM/L (normal range: 8–30 nM/L) and 65 nM/L (normal range: 78– 185 nM/L), respectively. An investigation into the composition of her TPN was subsequently undertaken. In consultation with inpatient pharmacists and nutritionists, her TPN was found to contain a composition of amino acids, dextrose, fat emulsion, calcium gluconate, magnesium sulfate, sodium chloride, sodium acetate, and potassium phosphate. There was no thiamine in the TPN mixture. Thus, given the clinical picture, we diagnosed the patient with iatrogenic Wernicke encephalopathy secondary to dietary thiamine depletion. Our patient was treated with 3 days of high-dose thiamine administered intravenously (500 mg every 8 hours) and transitioned to oral supplementation. After 5 days of repletion, her visual symptoms resolved. Although weakness improved, she still required the use of a rolling walker for ambulation when discharged. With resolution of her nausea and vomiting, we were able to remove her peripherally inserted central catheter on hospital day 7. Outpatient follow-up with neurology, maternal–fetal medicine, and physical therapy was arranged along with continued daily oral thiamine supplementation. A follow-up assessment of her thiamine level 3 weeks after discharge revealed normalization (49 nM/L), and the patient’s clinical response was monitored by her primary obstetrician.
DISCUSSION Treatment options for hyperemesis gravidarum range from oral antiemetic therapy to inpatient admission for intravenous medications and fluid resuscitation. Rarely, hyperemesis gravidarum requires TPN, with the goal of providing nutritional support to both mother and fetus until the patient is able to tolerate oral alimentation. When TPN is used to treat hyperemesis gravidarum, it has been associated with improved maternal nutritional status and varied effects on neonatal outcomes.3,4,6 However, TPN is not without complications. The overall complication rate is as high as 63%, which includes issues related to central catheter placement such as infections, mechanical failure, thromboses, hematomas, pneumothoraces, and cardiac arrhythmias.3,7–10 Additionally, the TPN mixture itself may evoke disturbances
VOL. 125, NO. 5, MAY 2015
in glycemic control, electrolyte imbalances, nutrient deficiencies, refeeding syndrome, hepatic dysfunction, and metabolic bone dysfunction, including osteomalacia and osteoporosis.10 With symptoms including nystagmus, ataxia, and mental status changes, Wernicke encephalopathy results from a deficiency of thiamine, an essential watersoluble vitamin with a relatively short half-life of 10–20 days.11,12 The total amount of stored thiamine in the average adult is approximately 30 mg.13 Thus, secondary to its short half-life and limited store, daily dietary thiamine intake is necessary.13 Additionally, the thiamine requirement increases in pregnancy and lactation to 1.4 mg per day, an increase of 0.3 mg per day from the baseline female requirement.13 In 2006, Selitsky et al and Chiossi et al reported and subsequently reviewed 45 and 49 cases, respectively, of Wernicke encephalopathy in the setting of hyperemesis gravidarum.2,5 Interestingly, Selitsky et al5 commented on the possibility that prompt treatment with total parenteral nutrition and vitamin supplementation could prevent thiamine deficiency in pregnancy. Conversely, as documented in our case, thiamine-deficient TPN either exacerbated or caused the deficiency leading to Wernicke encephalopathy. Moreover, nutritional deficiencies and cases of Wernicke encephalopathy have occurred in nonpregnant patients receiving TPN secondary to a lack of thiamine repletion, indicating the imperfect nature of TPN as a mode of full nutritional support.14,15 Our patient essentially combined two clinical scenarios that have both separately been associated with the development of Wernicke encephalopathy: hyperemesis gravidarum and total parenteral nutrition. The composition of TPN can actually be quite complex. Few commercial formulations of TPN are available because most formulations are compounded by pharmacies to provide patient-specific nutrition based on the clinical scenario.16,17 Thus, although guidelines for TPN formulation exist (based on calculated energy expenditure and estimated losses), TPN compositions are not standardized.16,17 Highlighting this lack of standardization, the American Society for Parenteral and Enteral Nutrition specifically addresses thiamine supplementation for pregnant women affected by hyperemesis gravidarum.18 We therefore recommend confirming the addition of a daily multivitamin that includes thiamine. A high index of suspicion is warranted in patients with hyperemesis gravidarum receiving TPN. Importantly, TPN is imperfect and should not be considered a “cure-all” for hyperemesis gravidarum. A thorough review of the patient’s medications, supplementations, and TPN orders is indicated in all patients. In the
Giugale et al
Wernicke Encephalopathy in Pregnancy 1151
Copyright ª by The American College of Obstetricians and Gynecologists. Published by Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
treatment of hyperemesis gravidarum, care should be taken to ensure adequate supplementation of thiamine to minimize the advent of any maternal and possible fetal morbidity. REFERENCES 1. Nausea and vomiting of pregnancy. ACOG Practice Bulletin No. 52. American College of Obstetricians and Gynecologists. Obstet Gynecol 2004;103:803–15. 2. Chiossi G, Neri I, Cavazzuti M, Basso G, Facchinetti F. Hyperemesis gravidarum complicated by Wernicke encephalopathy: background, case report, and review of the literature. Obstet Gynecol Surv 2006;61:255–68. 3. Holmgren C, Aagaard-Tillery KM, Silver RM, Porter TF, Varner M. Hyperemesis in pregnancy: an evaluation of treatment strategies with maternal and neonatal outcomes. Am J Obstet Gynecol 2008;198:56.e1–4. 4. Levine MG, Esser D. Total parenteral nutrition for the treatment of severe hyperemesis gravidarum: maternal nutritional effects and fetal outcome. Obstet Gynecol 1988;72:102–7. 5. Selitsky T, Chandra P, Schiavello HJ. Wernicke’s encephalopathy with hyperemesis and ketoacidosis. Obstet Gynecol 2006; 107:486–90. 6. Peled Y, Melamed N, Hiersch L, Pardo J, Wiznitzer A, Yogev Y. The impact of total parenteral nutrition support on pregnancy outcome in women with hyperemesis gravidarum. J Matern Fetal Neonatal Med 2014;27:1146–50. 7. Russo-Stieglitz KE, Levine AB, Wagner BA, Armenti VT. Pregnancy outcome in patients requiring parenteral nutrition. J Matern Fetal Med 1999;8:164–7.
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8. Ogura JM, Francois KE, Perlow JH, Elliott JP. Complications associated with peripherally inserted central catheter use during pregnancy. Am J Obstet Gynecol 2003;188:1223–5. 9. Nuthalapaty FS, Beck MM, Mabie WC. Complications of central venous catheters during pregnancy and postpartum: a case series. Am J Obstet Gynecol 2009;201:311.e1–5. 10. Maroulis J, Kalfarentzos F. Complications of parenteral nutrition at the end of the century. Clin Nutr 2000;19:295–304. 11. Higdon J, Drake V. An evidence-based approach to vitamins and minerals: health benefits and intake recommendations. 2nd ed. New York (NY): Thieme; 2012. 12. Machlin LJ. Handbook of vitamins: nutritional, biochemical, and clinical aspects. New York (NY): Marcel Dekker; 1984. 13. Biesalski HK, Grimm P, Junkermann S. Pocket atlas of nutrition. Revised translation of 3rd German ed. New York (NY): Thieme; 2005. 14. Francini-Pesenti F, Brocadello F, Manara R, Santelli L, Laroni A, Caregaro L. Wernicke’s syndrome during parenteral feeding: not an unusual complication. Nutrition 2009;25: 142–6. 15. Long L, Cai XD, Bao J, Wu AM, Tian Q, Lu ZQ. Total parenteral nutrition caused Wernicke’s encephalopathy accompanied by wet beriberi. Am J Case Rep 2014;15:52–5. 16. UpToDate. Total parenteral nutrition: drug information. www. uptodate.com. Retrieved August 31, 2014. 17. Longo DL, Harrison TR. Harrison’s principles of internal medicine. 18th ed. New York (NY): McGraw-Hill; 2012. 18. Guidelines for the use of parenteral and enteral nutrition in adult and pediatric patients. JPEN J Parenter Enteral Nutr 2002;26:1–138SA.
Wernicke Encephalopathy in Pregnancy
OBSTETRICS & GYNECOLOGY
Copyright ª by The American College of Obstetricians and Gynecologists. Published by Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Iatrogenic Wernicke Encephalopathy in a Patient With Severe Hyperemesis Gravidarum Lauren E. Giugale, MD, Omar M. Young, MD, and David C. Streitman,
MD
BACKGROUND: Hyperemesis gravidarum complicates 0.5–2.0% of pregnancies and may lead to substantial nutritional deficiencies. Total parenteral nutrition can be used in severe cases in an attempt to avoid such deficiencies. Rarely, thiamine deficiency resulting in Wernicke encephalopathy occurs, with significant maternal morbidity. CASE: We present the case of a 30-year-old woman with hyperemesis gravidarum at 13 4/7 weeks of gestation treated with prolonged total parenteral nutrition that lacked thiamine supplementation, resulting in iatrogenic Wernicke encephalopathy. After high-dose intravenous thiamine repletion, she experienced slow resolution of her symptoms. CONCLUSION: Pregnancies complicated by hyperemesis gravidarum treated with total parenteral nutrition represent potential high-risk clinical scenarios for thiamine deficiency. Compositions of total parenteral nutrition are not standardized. Thus, physicians must confirm repletion of all essential components to avoid significant morbidity. (Obstet Gynecol 2015;125:1150–2) DOI: 10.1097/AOG.0000000000000557
H
yperemesis gravidarum, a severe form of pregnancy-associated nausea and vomiting, affects 0.5–2.0% of all pregnancies.1 Symptoms of hyperemesis gravidarum include the following: persistent vomiting, ketonuria, weight loss of at least 5% of prepregnancy
From the Department of Obstetrics, Gynecology and Reproductive Sciences and the Division of Maternal-Fetal Medicine, Department of Obstetrics, Gynecology and Reproductive Sciences, Magee-Womens Hospital and University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania. Corresponding author: Lauren E. Giugale, MD, Department of Obstetrics, Gynecology and Reproductive Sciences, Magee-Womens Hospital and University of Pittsburgh Medical Center, 300 Halket Street, Pittsburgh, PA 15213; e-mail: [email protected]. Financial Disclosure The authors did not report any potential conflicts of interest. © 2015 by The American College of Obstetricians and Gynecologists. Published by Wolters Kluwer Health, Inc. All rights reserved. ISSN: 0029-7844/15
1150
VOL. 125, NO. 5, MAY 2015
Teaching Points 1. Hyperemesis gravidarum requiring total parenteral nutrition should be considered a high-risk clinical scenario for nutritional deficiency. 2. Total parenteral nutrition is not standardized; physicians must take responsibility to ensure that a multivitamin, including thiamine, is incorporated in the treatment of hyperemesis gravidarum. 3. This case report adds to the known risks associated with total parenteral nutrition delivered through a peripherally inserted central catheter in pregnancy, and further supports the goal of using alternative methods to provide nutrition in this setting.
weight, electrolyte disturbances, and abnormalities of thyroid and liver function tests.1 In refractory hyperemesis, obstetricians may use total parenteral nutrition (TPN) to improve maternal nutritional status until the patient is able to tolerate oral alimentation. Rarely, Wernicke encephalopathy can result from nutritional thiamine deficiency in the setting of severe hyperemesis gravidarum.2–5 We present a case of Wernicke encephalopathy that developed secondary to lack of thiamine repletion during the course of TPN therapy and aim to underscore the nature of thiamine deficiency in the current case and the need for the selective and judicious use of TPN in pregnancy.
CASE A 32-year-old woman, gravida 4 para 2101 presented to an outside hospital at 13 2/7 weeks of gestation with persistent lethargy, weakness, ataxia, and blurred vision. Notably, she had been diagnosed with hyperemesis gravidarum at approximately 8 weeks of gestation. The condition was not controlled with conservative management, and TPN was initiated through a peripherally inserted central catheter. After 28 days of continuous TPN, she noted 7 days of subjectively worsening lethargy, blurred vision, and weakness requiring assistance with ambulation. Notably, all three prior pregnancies were complicated by hyperemesis gravidarum requiring hospitalization; she had received TPN only in her most recent antecedent pregnancy. Initial laboratory evaluation demonstrated normal electrolytes, anemia (hemoglobin 8.5 gm/dL), and mild thrombocytopenia (platelets 1453109/L). An electroencephalogram demonstrated dysrhythmia and diffuse delta activity, indicative of a moderate encephalopathy. A lumbar puncture and magnetic resonance imaging of the brain and neck were all negative. Before transfer to our facility at 13 4/7 weeks of gestation, her TPN was discontinued and she was given intravenous folic acid and thiamine supplementation.
OBSTETRICS & GYNECOLOGY
Copyright ª by The American College of Obstetricians and Gynecologists. Published by Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
On arriving at our institution, a neurologic examination was notable for psychomotor slowing. Although the patient’s cranial nerves were intact and symmetric, she exhibited prominent bilateral gaze-evoked nystagmus. Strength and sensory testing were normal, but coordination testing demonstrated slowing of finger-to-nose testing in bilateral upper extremities with mild right-side ataxia. Her gait was widebased, wavering, and unsteady. She was unable to stand upright in place for greater than 2 seconds and she could ambulate only with a two-person assist. Repeat electroencephalography was performed given these persistent encephalopathic features and again revealed generalized slowing consistent with a diffuse disturbance of cerebral function. Thiamine levels drawn at the outside hospital and at our institution returned critically low values of less than 7 nM/L (normal range: 8–30 nM/L) and 65 nM/L (normal range: 78– 185 nM/L), respectively. An investigation into the composition of her TPN was subsequently undertaken. In consultation with inpatient pharmacists and nutritionists, her TPN was found to contain a composition of amino acids, dextrose, fat emulsion, calcium gluconate, magnesium sulfate, sodium chloride, sodium acetate, and potassium phosphate. There was no thiamine in the TPN mixture. Thus, given the clinical picture, we diagnosed the patient with iatrogenic Wernicke encephalopathy secondary to dietary thiamine depletion. Our patient was treated with 3 days of high-dose thiamine administered intravenously (500 mg every 8 hours) and transitioned to oral supplementation. After 5 days of repletion, her visual symptoms resolved. Although weakness improved, she still required the use of a rolling walker for ambulation when discharged. With resolution of her nausea and vomiting, we were able to remove her peripherally inserted central catheter on hospital day 7. Outpatient follow-up with neurology, maternal–fetal medicine, and physical therapy was arranged along with continued daily oral thiamine supplementation. A follow-up assessment of her thiamine level 3 weeks after discharge revealed normalization (49 nM/L), and the patient’s clinical response was monitored by her primary obstetrician.
DISCUSSION Treatment options for hyperemesis gravidarum range from oral antiemetic therapy to inpatient admission for intravenous medications and fluid resuscitation. Rarely, hyperemesis gravidarum requires TPN, with the goal of providing nutritional support to both mother and fetus until the patient is able to tolerate oral alimentation. When TPN is used to treat hyperemesis gravidarum, it has been associated with improved maternal nutritional status and varied effects on neonatal outcomes.3,4,6 However, TPN is not without complications. The overall complication rate is as high as 63%, which includes issues related to central catheter placement such as infections, mechanical failure, thromboses, hematomas, pneumothoraces, and cardiac arrhythmias.3,7–10 Additionally, the TPN mixture itself may evoke disturbances
VOL. 125, NO. 5, MAY 2015
in glycemic control, electrolyte imbalances, nutrient deficiencies, refeeding syndrome, hepatic dysfunction, and metabolic bone dysfunction, including osteomalacia and osteoporosis.10 With symptoms including nystagmus, ataxia, and mental status changes, Wernicke encephalopathy results from a deficiency of thiamine, an essential watersoluble vitamin with a relatively short half-life of 10–20 days.11,12 The total amount of stored thiamine in the average adult is approximately 30 mg.13 Thus, secondary to its short half-life and limited store, daily dietary thiamine intake is necessary.13 Additionally, the thiamine requirement increases in pregnancy and lactation to 1.4 mg per day, an increase of 0.3 mg per day from the baseline female requirement.13 In 2006, Selitsky et al and Chiossi et al reported and subsequently reviewed 45 and 49 cases, respectively, of Wernicke encephalopathy in the setting of hyperemesis gravidarum.2,5 Interestingly, Selitsky et al5 commented on the possibility that prompt treatment with total parenteral nutrition and vitamin supplementation could prevent thiamine deficiency in pregnancy. Conversely, as documented in our case, thiamine-deficient TPN either exacerbated or caused the deficiency leading to Wernicke encephalopathy. Moreover, nutritional deficiencies and cases of Wernicke encephalopathy have occurred in nonpregnant patients receiving TPN secondary to a lack of thiamine repletion, indicating the imperfect nature of TPN as a mode of full nutritional support.14,15 Our patient essentially combined two clinical scenarios that have both separately been associated with the development of Wernicke encephalopathy: hyperemesis gravidarum and total parenteral nutrition. The composition of TPN can actually be quite complex. Few commercial formulations of TPN are available because most formulations are compounded by pharmacies to provide patient-specific nutrition based on the clinical scenario.16,17 Thus, although guidelines for TPN formulation exist (based on calculated energy expenditure and estimated losses), TPN compositions are not standardized.16,17 Highlighting this lack of standardization, the American Society for Parenteral and Enteral Nutrition specifically addresses thiamine supplementation for pregnant women affected by hyperemesis gravidarum.18 We therefore recommend confirming the addition of a daily multivitamin that includes thiamine. A high index of suspicion is warranted in patients with hyperemesis gravidarum receiving TPN. Importantly, TPN is imperfect and should not be considered a “cure-all” for hyperemesis gravidarum. A thorough review of the patient’s medications, supplementations, and TPN orders is indicated in all patients. In the
Giugale et al
Wernicke Encephalopathy in Pregnancy 1151
Copyright ª by The American College of Obstetricians and Gynecologists. Published by Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
treatment of hyperemesis gravidarum, care should be taken to ensure adequate supplementation of thiamine to minimize the advent of any maternal and possible fetal morbidity. REFERENCES 1. Nausea and vomiting of pregnancy. ACOG Practice Bulletin No. 52. American College of Obstetricians and Gynecologists. Obstet Gynecol 2004;103:803–15. 2. Chiossi G, Neri I, Cavazzuti M, Basso G, Facchinetti F. Hyperemesis gravidarum complicated by Wernicke encephalopathy: background, case report, and review of the literature. Obstet Gynecol Surv 2006;61:255–68. 3. Holmgren C, Aagaard-Tillery KM, Silver RM, Porter TF, Varner M. Hyperemesis in pregnancy: an evaluation of treatment strategies with maternal and neonatal outcomes. Am J Obstet Gynecol 2008;198:56.e1–4. 4. Levine MG, Esser D. Total parenteral nutrition for the treatment of severe hyperemesis gravidarum: maternal nutritional effects and fetal outcome. Obstet Gynecol 1988;72:102–7. 5. Selitsky T, Chandra P, Schiavello HJ. Wernicke’s encephalopathy with hyperemesis and ketoacidosis. Obstet Gynecol 2006; 107:486–90. 6. Peled Y, Melamed N, Hiersch L, Pardo J, Wiznitzer A, Yogev Y. The impact of total parenteral nutrition support on pregnancy outcome in women with hyperemesis gravidarum. J Matern Fetal Neonatal Med 2014;27:1146–50. 7. Russo-Stieglitz KE, Levine AB, Wagner BA, Armenti VT. Pregnancy outcome in patients requiring parenteral nutrition. J Matern Fetal Med 1999;8:164–7.
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8. Ogura JM, Francois KE, Perlow JH, Elliott JP. Complications associated with peripherally inserted central catheter use during pregnancy. Am J Obstet Gynecol 2003;188:1223–5. 9. Nuthalapaty FS, Beck MM, Mabie WC. Complications of central venous catheters during pregnancy and postpartum: a case series. Am J Obstet Gynecol 2009;201:311.e1–5. 10. Maroulis J, Kalfarentzos F. Complications of parenteral nutrition at the end of the century. Clin Nutr 2000;19:295–304. 11. Higdon J, Drake V. An evidence-based approach to vitamins and minerals: health benefits and intake recommendations. 2nd ed. New York (NY): Thieme; 2012. 12. Machlin LJ. Handbook of vitamins: nutritional, biochemical, and clinical aspects. New York (NY): Marcel Dekker; 1984. 13. Biesalski HK, Grimm P, Junkermann S. Pocket atlas of nutrition. Revised translation of 3rd German ed. New York (NY): Thieme; 2005. 14. Francini-Pesenti F, Brocadello F, Manara R, Santelli L, Laroni A, Caregaro L. Wernicke’s syndrome during parenteral feeding: not an unusual complication. Nutrition 2009;25: 142–6. 15. Long L, Cai XD, Bao J, Wu AM, Tian Q, Lu ZQ. Total parenteral nutrition caused Wernicke’s encephalopathy accompanied by wet beriberi. Am J Case Rep 2014;15:52–5. 16. UpToDate. Total parenteral nutrition: drug information. www. uptodate.com. Retrieved August 31, 2014. 17. Longo DL, Harrison TR. Harrison’s principles of internal medicine. 18th ed. New York (NY): McGraw-Hill; 2012. 18. Guidelines for the use of parenteral and enteral nutrition in adult and pediatric patients. JPEN J Parenter Enteral Nutr 2002;26:1–138SA.
Wernicke Encephalopathy in Pregnancy
OBSTETRICS & GYNECOLOGY
Copyright ª by The American College of Obstetricians and Gynecologists. Published by Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
![[Wernicke encephalopathy complicating hyperemesis gravidarum and associated with pontine myelinolysis].](/assets/img/hold.png)
